ReviewHernia : the journal of hernias and abdominal wall surgery2011
The Nyhus-Wantz lectureship: etiology, herniosis, diverticulosis coli, and cancer.
Review in Hernia : the journal of hernias and abdominal wall surgery, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
5 citing papers in PubMed, 12 citations in OpenAlex.
- The impact of preoperative optimization for abdominal wall reconstruction on long-term glucose control and smoking cessation.Surgical endoscopy · 2025Article
- Cranial approach for preperitoneal/pretransversalis enhanced-view totally extraperitoneal (PeTEP) hernia repair: a novel technique description and early outcomes.Surgical endoscopy · 2025Observational
- Outcomes of surgically managed recurrent parastomal hernia: the Sisyphean challenge of the hernia world.Hernia : the journal of hernias and abdominal wall surgery · 2021Article
- Comments on Saint's triad.Surgical case reports · 2015Article
- A rare case of interparietal incisional hernia from 8 mm trocar site after robot-assisted laparoscopic prostatectomy.Hernia : the journal of hernias and abdominal wall surgery · 2014Article
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Authors and funding
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Funding
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Abstract
The Nyhus-Wantz Lectureship honors two giants who represent the few who formed a new surgical specialty: herniology. My topics are etiology, herniosis, diverticulosis coli, and cancer. Hippocrates blamed wear and tear for herniation. Russell's (Lancet 1:1519-1523, 1902) explanation was congenital peritoneal "buds" extending down to the pelvis. Harrison (Arch Surg 4:680-689, 1922) attributed herniae to transversalis fascial degradation. Keith (Lancet 2(17):1398-1399, 1906) concluded that pathology was involved, even though Russell (Lancet 1:1519-1523, 1902) had denied it. Nevertheless, the congenital theory prevailed. According to McVay (Christopher's textbook of surgery, W.B. Saunders, Philadelphia, 1960, p. 159), defects arise in normal musculo-aponeurotic structures. Research showed that atrophy was caused by damaged fibroblasts producing less collagen, which was abnormal (having a reduced I/III ratio). The disease was systemic, later named herniosis. Nicotine addiction increased the incidence of herniation by an inflammatory process named metastatic emphysema. In 1948, Saint's Triad, an aggregation of hiatus hernia (later, any primary hernia), gallstones, and diverticulosis coli, was introduced. This association occurred eight times more often than expected, with herniosis appearing to be its cause, abetted by high blood cholesterol causing gallstones. In 2006, Krones et al. (Int J Colorectal Dis 21:18-24, 2006) provided evidence that colon cancer is accompanied by a reduction in diverticula. Klinge et al. (Hernia 8(4):300-301, 2004) showed that these entities require different extracellular matrices (ECMs). Ghajar and Bissell (Histochem Cell Biol 130:1105-1118, 2008) pointed out that the ECM, which comprises 80% of the breast, influences its epithelial genetic expression, likewise with other organs (kidney, skin, lung, colon, and ovaries). Recently, a fundamental change in our understanding of cancer growth and metastasis has taken place. Whereas the degradation of connective tissue was thought to encourage invasion, eliciting concern for the herniated, now, investigators report the reverse, a reactive vascularized stroma resembling wound healing with an increase in fibroblasts and collagen I. Words such as desmoplasia, fibrosis, and stiffening abound. In conclusion, degradation of the ECM may be why herniosis appears to be hostile to the development of cancer throughout the body. Studies are needed of patients with and without a history of hernia to determine their incidence of cancer. Data from smokers should be separated, since they carry their own high risk of malignancy.
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Registered trials
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